Human bronchial explants activated benzo(a)pyrene and 7,8-diol into proximate and ultimate carcinogenic metabolites that were then released into the medium containing the cocultivated Chinese hamster V-79 cells; and increase in mutation frequency of indicator V-79 cells was observed. With the new fluorescent plus Giemsa staining method, there was also an increase in sister chromatid exchanges (SCE) in the cocultivated V-79 cells. In addition to causing a higher increase of mutation frequency mediated by human bronchus than benzo(a)pyrene, 7,8-diol showed a higher increase of SCE in cocultivated V-79 cells. 7,8-Benzoflavone, an inhibitor of the metabolism of polynuclear aromatic hydrocarbon, also inhibited bronchial explant-mediated SCE and mutation in the indicator V-79 cells. Benzo(e)pyrene, the weakly carcinogenic analog of benzo(a)pyrene, did not increase either SCE or mutation frequency of V-79 cells. In addition to bronchial explants, pulmonary alveolar macrophage and blood monocytes have the capability to mediate mutation and SCE.